[Hypoglossal nerve injury following endotracheal intubation]. / Uitval van de N. hypoglossus na orotracheale intubatie.

BACKGROUND: Endotracheal intubation is required to keep the airway open when a patient undergoes surgery under general anaesthetic. Here we present a rare complication of endotracheal intubation. CASE: A 70-year-old woman underwent repeat pulmonary vein isolation for atrial fibrillation under general anaesthetic. Because the procedure was expected to take a long time, and because the surgeon might want to perform transoesophageal echocardiography, we chose to carry out endotracheal intubation on this patient. After the operation she showed dyspnoea, problems with swallowing and dysarthria. Physical examination showed elevation of the right pharyngeal arch and deviation of the tongue to the right. This was found to be due to hypoglossal nerve injury. CONCLUSION: Hypoglossal nerve injury is a rare complication of endotracheal intubation. There is no proven effective treatment for this complication. Prognosis is favourable: 69% of the patients recover completely in the first 6 months following intubation. Patients with this complication should receive supportive therapy, such as speech therapy and dietary modifications, to prevent aspiration.

Alcohol Intoxication as a Stroke Mimic and the Incidence of Acute Alcohol Intoxication in Stroke.

BACKGROUND AND AIM: Alcohol intoxication can be a posterior circulation stroke mimic as they share symptoms such as dysarthria, gait disturbances and nystagmus. We describe alcohol intoxication as a stroke mimic and the frequency of acute alcohol intoxication among stroke patients. METHODS: Prospective observational single-center study (2014-2017, Haga Ziekenhuis, the Hague). In all patients older than 16 years presenting as possible acute stroke less than 6 hours of onset, blood ethanol was measured; greater than 0.1 blood alcohol concentration (BAC) was considered elevated. RESULTS: In total 974 patients were included: 60 (6%) had elevated blood ethanol (mean: 1.3 BAC). In 180 of 974 patients (18%) a stroke mimic was diagnosed: 12 were due to alcohol intoxication (1% of total cohort, 7% of stroke mimic, mean ethanol level: 2.2 BAC). Half of these patients denied or downplayed their alcohol consumption. Stroke and concurrent alcohol intoxication occurred in 38 of 794 strokes (5%, mean ethanol level: 1.1 BAC). Compared to other stroke patients, these 38 patients presented more often after working hours (mean 6.38pm versus 2.23pm) and received alteplase and endovascular therapy less often (24% versus 43%, P = .018 and 3% versus 10%, P = .241, respectively). CONCLUSIONS: Of all patients presenting as possible acute stroke, 6% also drank alcohol. 18% of the whole cohort was diagnosed with a stroke mimic. Acute alcohol intoxication as sole diagnosis was diagnosed in 1% of the total cohort and 7% of stroke mimics, 50% denied or downplayed their alcohol consumption. 5% of all stroke patients also drank alcohol, they were significantly less likely to receive alteplase or endovascular treatment.

Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation.

Inflammation drives atherosclerotic plaque progression and rupture, and is a compelling therapeutic target. Consequently, attenuating inflammation by reducing local macrophage accumulation is an appealing approach. This can potentially be accomplished by either blocking blood monocyte recruitment to the plaque or increasing macrophage apoptosis and emigration. Because macrophage proliferation was recently shown to dominate macrophage accumulation in advanced plaques, locally inhibiting macrophage proliferation may reduce plaque inflammation and produce long-term therapeutic benefits. To test this hypothesis, we used nanoparticle-based delivery of simvastatin to inhibit plaque macrophage proliferation in apolipoprotein E deficient mice (Apoe-/- ) with advanced atherosclerotic plaques. This resulted in rapid reduction of plaque inflammation and favorable phenotype remodeling. We then combined this short-term nanoparticle intervention with an eight-week oral statin treatment, and this regimen rapidly reduced and continuously suppressed plaque inflammation. Our results demonstrate that pharmacologically inhibiting local macrophage proliferation can effectively treat inflammation in atherosclerosis.